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Numerous studies have found appraisals of pain as a source of potential threat or tissue damage influence pain perception and coping. Conversely, causal effects of challenge appraisals reflecting potential future benefits of bearing pain have received little attention. This experiment was designed to elucidate effects of appraising laboratory pain as a source of potential threat and challenge on pain perception and coping.
Before engaging in a cold pressor test (CPT), young adult women (N = 112) and men (N = 49) were randomly assigned to one of three conditions: a higher threat group in which participants read an orienting passage describing symptoms and consequences of frostbite (pain as a signal for nociception), a lower threat group in which participants read about CPT safety (pain independent of nociception) or a challenge appraisal group in which participants read a passage describing how persistence in the face of discomfort predicts future life success and satisfaction.
The higher threat group had lower pain tolerance and catastrophized more during the task than lower threat and challenge appraisal groups. Conversely, the challenge appraisal group reported using more cognitive strategies (ignoring, diverting attention, coping self-statements) in managing pain than either threat group. Structural equation modelling indicated paths of subjective threat and challenge appraisals with pain tolerance were fully mediated by individual differences in reported cognitive coping and/or pain catastrophizing.
Findings underscore causal effects of pain appraisals on coping responses and pain perception.
Effects of challenge appraisals of pain as a source of potential future growth or development have not been considered in experimental pain research.
Causal effects of primary appraisals of laboratory pain as a source of potential threat and challenge were elucidated in relation to pain perception and coping.
Widespread musculoskeletal pain (WSP) and obesity frequently co-occur and may have shared risk factors. We aimed to investigate whether four dichotomized risk factors individually or jointly increase the risk for the onset of WSP and onset of obesity.
Persons aged 34–76 years in 2004 living in Ullensaker municipality, Norway, responded to questionnaires in 2004 and 2010 (n = 1553). Using causal interaction analyses, we examined whether baseline obesity and WSP, poor sleep quality, mental distress and poor physical fitness jointly increased the risk of new onset WSP (≥3 pain sites leading to disability the last year) and new onset obesity (self-reported BMI ≥30 kg/m2) in persons without WSP (n = 1270) or without obesity (n = 1300) at baseline respectively.
The mean (SD) age was 51 (12.1) years and 56% were female. The incidence of WSP and obesity were 9.1% and 5.4%. Mental distress and poor sleep quality individually and jointly with poor physical fitness increased WSP onset risk (relative excess risk due to interaction [RERI] = 1.90, 95% CI, 0.39–3.42 and RERI = 1.43, 95% CI, 0.10–2.76). Poor physical fitness individually increased the risk for new onset obesity, and baseline WSP and poor sleep quality jointly (RERI = 1.87, 95% CI, 0.49–3.24). The presence of more risk factors was dose-dependently associated with onset WSP and to a lesser extent with onset obesity.
The onset of WSP and the onset of obesity were results of joint effects of exposures. Poor physical fitness was a key covariate in increasing the risk for both conditions.
In a general population, the new onset of widespread pain and new onset of obesity were results of joint effects of risk factors and particularly poor physical fitness.
The study may aid in the identification of patients at risk of future disability.
Fibromyalgia is a chronic widespread pain condition, with patients commonly reporting other symptoms such as sleep difficulties, memory complaints and fatigue. The use of magnetic resonance imaging (MRI) in fibromyalgia has allowed for the detection of neural abnormalities, with alterations in brain activation elicited by experimental pain and alterations in resting state connectivity related to clinical pain.
In this study, we sought to monitor state changes in resting brain connectivity following experimental pressure pain in fibromyalgia patients and healthy controls. Twelve fibromyalgia patients and 15 healthy controls were studied by applying discrete pressure stimuli to the thumbnail bed during MRI. Resting-state functional MRI scanning was performed before and immediately following experimental pressure pain. We investigated changes in functional connectivity to the thalamus and the insular cortex.
Acute pressure pain increased insula connectivity to the anterior cingulate and the hippocampus. Additionally, we observed increased thalamic connectivity to the precuneus/posterior cingulate cortex, a known part of the default mode network, in patients but not in controls. This connectivity was correlated with changes in clinical pain.
These data reporting changes in resting-state brain activity following a noxious stimulus suggest that the acute painful stimuli may contribute to the alteration of the neural signature of chronic pain.
In this study acute pain application shows an echo in functional connectivity and clinical pain changes in chronic pain.